Wei et al., have studied the subunit composition of γ-aminobutyric acid type A receptors responsible for the tonic inhibition of parvalbumin positive interneurons and identified a small molecule (DDL-920) as a potent, efficacious, and selective negative allosteric modulator of these receptors. DDL-920 increases the power of γ-oscillations following oral administration and remedies the memory impairment of Alzheimer’s disease model mice in the Barnes maze.
A therapeutic small molecule enhances γ-oscillations and improves cognition/memory in Alzheimer’s disease model mice
Not a lot of info on this new compound DDL-920 so I search for other possibly similar compounds using https://www.asklongevitygpt.com/
I find that this AI search engine provides good information but the references it provides in it’s reports are weird and not related to the information it provides, So i have to do a second step to double check the references. When I do that, I have, so far, found the information matches what I can find “manually”
General Information
γ-Oscillations and Cognitive Function
γ-Oscillations: These are high-frequency brain waves (30-100 Hz) associated with various cognitive processes, including attention, memory, and perception.
Cognitive Enhancement: Enhancing γ-oscillations has been linked to improved cognitive function and memory.
Small Molecules of Interest
Several small molecules have been studied for their potential to enhance γ-oscillations and cognitive function. Here are a few examples:
Donepezil:
Mechanism: Donepezil is an acetylcholinesterase inhibitor that increases acetylcholine levels in the brain, which can enhance γ-oscillations.
Studies: Research has shown that donepezil can improve cognitive function in patients with Alzheimer’s disease.
Memantine:
Mechanism: Memantine is an NMDA receptor antagonist that modulates glutamatergic neurotransmission, potentially affecting γ-oscillations.
Studies: Memantine has been found to improve cognitive function in Alzheimer’s disease patients.
They’ve been curing alzheimers in mouse models for decades… the models are not very good and typically don’t translate well to humans, so I don’t get too excited about this type of research. We’ll see…
Research has been focused on the Tau theory for the last 25 or 30 years and over $30B spent with nothing important to show for it. Not because “mouse”, but because of the politics of research funding. If you don’t subscribe to the Tau theory you don’t get research grants and Uni’s expect their top scientists to bring in research funding. So they toe the line on this one, as any research outside the line doesn’t get funding.
It seems like that is changing a bit with more focus on microbiome and other areas of interest. As evident by many calling AZ “type 3 diabetes” and looking at gylcemic control as well.
This is a new drug, not touted as a cure or preventative but something that may slow cognitive decline.
Like aging in general, until the actual cause of AZ is figured out, slowing it or finding ways to compensate for it are all we’ve got for now. The 2 drugs that have “similar” targets Donepezil and Memantine have shown memory benefits but are not a cure either.
I have been taking Donepezil+Memantine for a few weeks as I am old and I am using it as a prophylactic. Very cheap from India.
No adverse reactions so far and no subjective benefits. I have only been taking it for three weeks. It may take months for benefits to show up, or again, it may be just a prophylactic intervention.
